More than 55 million people across the globe live with Alzheimer disease (AD).1 In the United States alone, approximately 6.2 million Americans age 65 and older live with the neurodegenerative disease. This number is predicted to grow to 13.8 million by 2060 unless there is some sort of medical breakthrough.1
As the Baby Boomer population ages, the numbers of those with AD is expected to accelerate. So, there has never been a more pressing time for research on this type of dementia and what causes it. Fortunately, researchers are approaching the problem from many angles, including that of oral health.
PERIODONTAL PATHOGENS AND ALZHEIMER DISEASE
AD is characterized by the plaque-forming accumulation of the protein beta-amyloid and what are known as “neurofibrillary tangles” of the hyperphosphorylated protein tau in the brain. Phosphorylation refers to the transfer of phosphate molecules to a protein. Abnormally hyperphosphorylated tau becomes toxic and can lead to neuron death. These developments are considered the hallmarks of AD. Yet, it is unclear what causes this to happen.
Now a growing body of evidence indicates that periodontitis and the pathogens that cause it to pose a significant risk factor for AD. In fact, several studies have investigated the potential causative relationship between AD and Porphyromonas gingivalis, traces of which have been found in post-mortem brain samples. P. gingivalis has been found to increase pro-inflammatory mediators and beta-amyloid in the brains of animals, diminishing cognitive performance. But so far, results have been inconclusive.2
RESEARCH YIELDS NEW INSIGHTS
Recent studies are turning the spotlight on the periodontal pathogen Treponema denticola and the role it may play in AD’s pathology. Researchers have begun to connect T. denticola with the development of tau hyperphosphorylation in mice.3,4
One study investigated whether oral infection with T. denticola would cause tau hyperphosphylation in the hippocampi of mice. They found that orally administered T. denticola did, indeed, colonize the brain tissue, promoting the hyperphosphorylation of tau protein by activating neuroinflammation in the hippocampi of mice.3 Another study demonstrated that T. denticola was able to enter the brain and act directly on nerve cells resulting in intra- and extracellular beta-amyloid accumulation in the hippocampus in mice.4
NO TIME LIKE THE PRESENT
While both P. gingivalis and T. denticola are being increasingly linked to the development of AD, more research is needed to understand the mechanics of this interaction.
These and similar studies illustrate the importance of maintaining a high level of oral hygiene. Interdental cleaning is integral to promoting both systemic and oral health. Especially in the elderly and those with cognitive impairment, early detection of periodontal diseases and periodontal therapy are critical.
- Alzheimer’s Association. 2021 Alzheimer’s Disease Facts and Figures.
- Jungbauer G, Stähli A, Zhu X, Auber Alberi L, Sculean A, Eick S. Periodontal microorganisms and Alzheimer disease—a causative relationship. Periodontol 2000. 2022;89:59–82.
- Tang Z, Cheng X, Su X, Wu L, Cai Q, Wu H. Treponema denticola induces Alzheimer-like tau hyperphosphyorylation by activating hippocampal neuroinflammation in mice. J Dent Res. 2022;101:992–1001.
- Su X, Tang Z, Lu Z, et al. Oral treponema denticola infection induces Aβ1-40 and Aβ1-42 accumulation in the hippocampus of C57BL/6 mice. J Mol Neurosci. 2021;71:1506–1514.